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Fragment Length Polymorphism Methods (fragment + length_polymorphism_methods)
Selected AbstractsGlutathione S -transferase M3 (A/A) genotype as a risk factor for oral cancer and leukoplakia among Indian tobacco smokersINTERNATIONAL JOURNAL OF CANCER, Issue 1 2004Nilabja Sikdar Abstract Polymorphism in glutathione S -transferase (GST) genes, causing variations in enzyme activities, may influence susceptibility to oral cancer and leukoplakia in smokers and/or smokeless tobacco users. In this case-control study consisting of 109 leukoplakia and 256 oral cancer patients and 259 controls, genotype frequencies at GSTM1, GSTT1, GSTM3 and GSTP1 loci were determined by polymerase chain reaction-restriction fragment length polymorphism methods and analyzed by multiple logistic regression to determine the risks of the diseases. There were no significant differences in the distributions of GSTM1, GSTM3 and GSTT1 genotypes in patients and controls when all individuals were compared. In contrast, frequencies of ile/ile genotype at codon 105 and variant val-ala haplotype of GSTP1 was significantly higher (OR = 1.5; 95% CI = 1.0,2.0) and lower (OR = 1.4; 95% CI = 1.0,1.9) in oral cancer patients compare to controls, respectively. The impacts of all genotypes on risks of oral cancer and leukoplakia were also analyzed in patients with different tobacco habits and doses. Increased risks of cancer and leukoplakia were observed in tobacco smokers with GSTM3 (A/A) genotype (OR = 2.0, 95% CI = 1.0,4.0; OR = 2.0, 95% CI = 1.0,4.4, respectively). So, GSTM3 (A/A) genotype could become one of the markers to know which of the leukoplakia would be transformed into cancer. Heavy tobacco chewing (> 124 chewing-year) increased the risk of cancer in individuals with GSTT1 homozygous null genotype (OR = 3.0; 95% CI = 1.0,9.8). Furthermore, increased lifetime exposure to tobacco smoking (> 11.5 pack-year) increased the risk of leukoplakia in individuals with GSTM1 homozygous null genotype (OR = 2.4; 95% CI = 1.0,5.7). It may be suggested that polymorphisms in GSTP1, GSTM1, GSTM3 and GSTT1 genes regulate risk of cancer and leukoplakia differentially among different tobacco habituals. © 2003 Wiley-Liss, Inc. [source] Study: The Lack of Significant Association of the Catechol- O -Methyl Transferase (COMT) Gene Polymorphism in Violent Offenders with Mental RetardationJOURNAL OF FORENSIC SCIENCES, Issue 1 2010Aysun Baransel Isir M.D. Abstract:, Little is known about criminality of cognitively impaired people and also there have been no reports on the relationship between catechol- O -methyl transferase (COMT) and committed Mental Retardation (MR) subjects. In the present study, the association between committed (violent offences) MR subjects and genetic variants of COMT were investigated by using polymerase chain reaction and based restriction fragment length polymorphism methods. During 6 years of follow-up, 36 violent offenders with mild MR were investigated. Thirty-six control volunteers were included in the study as a control group. H/L polymorphism of the COMT gene was investigated in these two groups. In conclusion, the COMT gene genotype distribution and allele frequency is not significantly different between the two groups (p > 0.05). This result suggests that the H/L polymorphism of the COMT gene does not show an association with the potential of "commits-violent offense" of Turkish subjects with mental retardation, compared with control group. [source] CTLA-4 gene promoter and exon 1 polymorphisms in Iranian patients with gastric and colorectal cancersJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2007Abolghasem Hadinia Abstract Background and Aim:, Cytotoxic T-lymphocyte antigen-4 (CTLA-4) is a potent immunoregulatory molecule that suppresses antitumor response by down-regulating T-cell activation. Effects of several polymorphisms in CTLA-4 on CTLA-4 expression and function have been previously documented. The aim of this study was to investigate the putative effect of CTLA-4 polymorphisms on susceptibility to gastric and colorectal cancers in an Iranian population. Methods:, A total of 155 patients (109 with colorectal cancer and 46 with gastric cancer) and 190 age- and sex-matched healthy controls were evaluated. Genotyping of ,1722T/C, ,1661A/G, and +49A/G were performed by PCR restriction fragment length polymorphism methods and of ,318C/T by a PCR amplification refractory mutation system technique. Results:, No statistically significant differences were found in the genotype distribution and allele frequencies among patients and controls. Haplotype analysis demonstrated that the TACG haplotype (,1722T, ,1661A, ,318C, +49G) frequency was significant increased in patients with colorectal cancer (P = 0.009) and gastric cancer (P = 0.006) in comparison to the control group. In contrast, the TACA haplotype frequency was significantly decreased in patients with colorectal cancer (P = 0.02) and not significantly decreased in patients with gastric cancer (P = 0.13) compared to the control group. Conclusion:, A positive association between CTLA-4 TACG haplotype and gastric and colorectal cancers was found in an Iranian population. A protective role for TACA haplotype is postulated. [source] Genetic Determinants of Alcohol Addiction and Metabolism: A Survey in ItalyALCOHOLISM, Issue 2 2001Roberta Pastorelli Background: Although multiple genes are involved in alcoholism and can contribute differently to the risk of dependence and liver damage, no studies have investigated susceptibility to addiction in combination with susceptibility to liver damage due to differences in ethanol metabolism. Methods: We evaluated the role of three polymorphic genes related to alcohol metabolism (CYP2E1) and, possibly, dependence (DRD2 and SLC6A4 promoter) in a series of 60 alcoholics admitted to a specialized referral center in Florence, Italy. Eighteen had a diagnosis of liver cirrhosis. A control series of 64 blood donors were identified at the same hospital. Genotyping was done by polymerase chain reaction-restriction fragment length polymorphism methods. Results: No difference was found in the frequency of the CYP2E 1 Rsa I c2 allele (2.5% among alcoholics and 4.7% among controls) and the Dra I C allele (6.7% and 10.1%). Similarly, no difference was found in the frequency of the DRD2 A1 allele (15.8% and 13.3%) and the B1 allele (10.8% and 8.6%). The proportion of controls with a combined B1 genotype (B1/B1 or B1/B2) was significantly associated with smoking (p= 0.03). The distribution of the S and L allele of the SLC6A4 gene was similar in the two groups, with 15% and 14%, respectively, homozygous S/S carriers. A significant association, however, emerged in the group of alcoholics, with a five times higher risk for S/S carriers of developing cirrhosis (p < 0.05). This association with liver persisted even after exclusion of the subgrouped of 10 hepatitis C virus positive alcoholics. Conclusions: Overall, our results provided no evidence of an increased susceptibility to develop alcoholism that was associated with the three genotypes investigated, either alone or in combination. An increased risk of developing liver cirrhosis for S/S homozygous carriers among alcohol-dependent patients was observed for the first time. [source] | ||||||||||